Following traumatic, paralyzing spinal cord injury (SCI), there is a marked reduction in local blood flow that is correlated with ischemia, hypoxia and eventual nervous tissue cell death (Hemorrhagic necrosis, HN). This laboratory has hypothesized that SCI results in an excessive local release of norepinephrine (NE) from nerve terminals associated with spinal cord parenchyma and blood vessels which induces vasoconstriction of the microvasculature, and the resultant stasis and related events. Our study object is to biochemically test this hypothesis. Experiments have been designed to determine the SCI effects on NE synthesis, release and utilization (turnover). Additional experiments have been designed to conversely determine the effects of NE per se on regional cord HN, blood flow, edema and amino acids. The first studies coupled a radioenzymatic NE assay capable of picogram sensitivity with two sensitive turnover methods. These methods utilize the direct 3HDA precursor of NE given by two different routes in the adult cat. The turnover will be measured by following the specific activity of the 3HNE product decay curve in injured vs non-injured control cats. The second experiments will examine the effect of SCI on pathophysiologic parameters (above) in cats previously NE depleted with six-hydroxydopamine. Preliminary data from studies in progress indicate that there is an increased turnover in several discrete regions within the injury site vicinity and that there is a substantial release of NE in conjunction with this turnover. These studies are consistent with our hypothesis, and suggest that NE may play an etiologic role in vascular stasis and nerve tissue death. Furthermore, data from the AA studies indicate that the all important white matter is biochemically intact for at least one hour following SCI, in agreement with anatomic studies by this and other laboratories.